Effects of Ethanol and Naltrexone in a Model of Traumatic Brain Injury With Hemorrhagic Shock

Abstract

In this TBI/HS model, NTX reverses ethanol-induced depression of hypercapnic ventilatory response but does not improve MAP, CPP, or metabolic acidosis. This suggests that the respiratory effects of ethanol in TBI, but not the hemodynamic effects, may be mediated by opiate receptor activation.

Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

“…In this clinical study, blood glucose in the hypothermia group was 100% less than 10 mmol/L, compared to 75.6% in the normothermia group after 3 days of treatment, which may be associated with the better recovery observed in patients [86]. Second, the application of naloxone, an opioid receptor antagonist, may effectively exert anti-inflammatory effects and improve the metabolism of brain cells in the early stages of severe TBI; on the other hand, naloxone also relieves calcium overload and prevents the toxicity of excitatory amino acids [87, 88]. Third, mannitol or hypertonic saline administration are effective ways of decreasing hyperpermeability and raised ICP induced by hyperglycemia after severe TBI [89, 90].…”

Laboratory Models Available to Study Alcohol‐Induced Organ Damage and Immune Variations: Choosing the Appropriate Model

“…Animals have free access to rodent chow and water. Alcohol or the vehicle is administered IV as a bolus injection followed by a continuous infusion via a catheter implanted in jugular, femoral, or cephalic vein Gilliam, 1989;Wilkinson and Rheingold, 1981;Zink et al, 2001).…”

“…The model has been used to study hypothermic, tolerance (Gilliam, 1989), metabolic (D'Souza et al, , 1992Molina et al, 1989Molina et al, , 1991 hemodynamic (Molina et al, 2004;Zink et al, 2001), immunological (Bautista, 2002a,b;Bautista et al, 1991), and neuroendocrine (Molina et al, 2004) changes induced by acute alcohol intoxication alone and in association with a Second Hit in numerous organs including liver (Bautista, 2002a,b;Spitzer and Zhang, 1996), muscle (Pagala et al, 1995;Vary and Lang, 2008), blood (Spitzer and Zhang, 1996), brain (Pawlosky et al, 2010), and the lung (Spitzer et al, 2002).…”

Effects of ethanol on limited resuscitation in a model of traumatic brain injury and hemorrhagic shock

“…Immature swine have cardiovascular, cerebrovascular, hematological, and electrolyte profiles almost identical to those in young humans. 20,51,[53][54][55][56][57][58] A fluid-percussion injury model was chosen because it has been studied extensively, is highly reproducible, and incorporates secondary injury. 6,7,11,13,22,27,29,35,47 Hemorrhage was initially induced in a controlled manner from a femoral artery catheter connected to a computerized roller pump.…”